Frontiers in Cardiovascular Medicine最新文献

{"title":"Myocardial dysfunction caused by MyBPC3 P459fs mutation in hypertrophic cardiomyopathy: evidence from multi-omics approaches and super-resolution imaging.","authors":"Yupeng Wu, Yuzhu Zhang, Qirui Zheng, Qiyuan Wang, Xingyu Fang, Zaihan Zhu, Jing Lu, Dandan Sun","doi":"10.3389/fcvm.2025.1529921","DOIUrl":"10.3389/fcvm.2025.1529921","url":null,"abstract":"<p><strong>Introduction: </strong>Mutations in the sarcomere protein, particularly in cardiac myosin binding protein C gene (<i>MyBPC3</i>), were the most frequent genetic cause of hypertrophic cardiomyopathy (HCM). The pathogenic MyBPC3 P459fs mutation has been reported in HCM patients. However, there was limited knowledge of the structure-function relationships and potential pathways in clinical HCM with MyBPC3 P459fs mutation.</p><p><strong>Methods: </strong>We used multi-omics approaches and super-resolution imaging to explore the effects of MyBPC3 P459fs mutation on humans and cells. HCM patients carrying MyBPC3 P459fs mutation (MyBPC3-P459fs HCMs) and healthy controls (HCs) were evaluated for myocardial function using both conventional and advanced echocardiography. In parallel, H9C2 myocardial cells infected with either MyBPC3 P459fs mutation (P459fs cells) or its wild type (WT cells) were investigated for myocardial fiber formation and the potential pathways behind this using super-resolution imaging and metabolomics and proteomics.</p><p><strong>Results: </strong>First, conventional and advanced echocardiography showed that MyBPC3-P459fs HCMs exhibited left ventricular diastolic and systolic dysfunction. Subsequently, super-resolution imaging indicated that P459fs cells formed fewer and shorter myocardial fibers in the cytoplasm compared to WT cells. Moreover, our metabolomic and proteomic data suggested several key components of mitochondrial membrane integrity, myocardial remodeling, myocardial energy metabolism, oxidative stress, inflammation, and actin binding capacity were significantly altered in response to P459fs mutation.</p><p><strong>Conclusions: </strong>This investigation indicated myocardial dysfunction and myocardial fiber disarray in clinical HCMs with MyBPC3 P459fs mutation and added potential pathways underlying this. These findings provided a link between the observed structural and functional disorders in MyBPC3 P459fs mutation and its onset of HCM pathogenesis and might have a significant translational contribution to effective treatment in HCM patients with MyBPC3 P459fs mutation.</p>","PeriodicalId":12414,"journal":{"name":"Frontiers in Cardiovascular Medicine","volume":"12 ","pages":"1529921"},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903464/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myocardial intramural course may reduce left ventricular ejection fraction of patients suffering from coronary heart disease.","authors":"Shi Miaomiao, Zheng Jiaqi, Li Xiaomeng, Li Shanshan, Wang Jie, Liu Kaicheng, Jia Mei, Su Ming","doi":"10.3389/fcvm.2025.1451173","DOIUrl":"10.3389/fcvm.2025.1451173","url":null,"abstract":"<p><strong>Background: </strong>Myocardial intramural course (MIC), a benign anatomical lesion, is an abnormal anatomical structure formed due to abnormal blood vessel routing. An increasing number of studies indicate that MIC is associated with coronary heart disease (CHD). However, it remains unclear whether MIC contributes to cardiac function impairment in patients with CHD. Thus, this study is to observe the association between MIC and cardiac function in patients with CHD.</p><p><strong>Methods: </strong>All participants were recruited from the Department of Cardiology, Peking University People's Hospital from August 2022 to September 2023. A total of 126 patients were diagnosed with MIC by coronary angiography and/or coronary CT angiography. Among them, a total of 39 patients diagnosed with MIC and CHD were enrolled in the MIC-CHD group. Sixty cases of monthly stratified CHD patients were randomly selected, into the CHD group as controls.</p><p><strong>Results: </strong>The left ventricular ejection fraction (LVEF) of patients in the MIC-CHD group was lower than that in the CHD group (0.62 vs. 0.67, <i>p</i> = 0.0153). LVEF in patients of MIC-CHD was negatively correlated with the systolic stenosis degree of mural coronary artery (MCA) (<i>r</i> = -0.6474, <i>p</i> = 0.0123) and MIC length (<i>r</i> = -0.5712, <i>p</i> = 0.0414).</p><p><strong>Conclusions: </strong>The combination of MIC in patients with CHD may contribute to the reduction of LVEF, whereas MIC length and the systolic stenosis degree of MCA were negatively correlated with LVEF.</p>","PeriodicalId":12414,"journal":{"name":"Frontiers in Cardiovascular Medicine","volume":"12 ","pages":"1451173"},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pulsed field ablation for atrial fibrillation: a comprehensive bibliometric analysis of research trends and emerging Frontiers.","authors":"Li Li, Bin Xie","doi":"10.3389/fcvm.2025.1513942","DOIUrl":"10.3389/fcvm.2025.1513942","url":null,"abstract":"<p><strong>Background: </strong>Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia worldwide, posing significant health burdens. Pulsed field ablation (PFA) is an emerging non-thermal technique that is gaining traction due to the ability to selectively target myocardial cells and minimize damage to surrounding tissues. We conducted a comprehensive bibliometric analysis of PFA use in AF treatment to map research trends, collaborations, and future directions.</p><p><strong>Methods: </strong>We extracted data from the Web of Science Core Collection on September 6, 2024, using search terms related to PFA and AF. Publication trends, citation trajectories, collaborative networks, and keyword co-occurrences were analyzed utilizing tools such as Bibliometrix R, VOSviewer, and CiteSpace.</p><p><strong>Results: </strong>In total, 217 publications were retrieved. The number of publications increased rapidly from 2019 to 2024, with a notable surge occurring after 2022. Contributions from the United States, Germany, and China accounted for more than 60% of all publications. The institution with the largest output was The Icahn School of Medicine at Mount Sinai. The most productive journals were <i>Europace</i> and the <i>Journal of Interventional Cardiac Electrophysiology</i>. Prolific authors were identified, underscoring significant international collaborations. The most cited publications highlighted the efficacy and safety of PFA. Keywords with strong recent citation bursts included \"tissue\", \"cardiomyopathy\", and \"closed chest ablation\".</p><p><strong>Conclusion: </strong>PFA is becoming established as a viable alternative for AF ablation, showing promising safety and efficacy. This bibliometric analysis confirmed the growing scientific interest and collaborative efforts in this field, suggesting that robust future developments will occur.</p>","PeriodicalId":12414,"journal":{"name":"Frontiers in Cardiovascular Medicine","volume":"12 ","pages":"1513942"},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903418/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interventional closure of artificial vascular anastomotic fistula after aortic replacement: a case report.","authors":"Qingwang Hou, Tongfeng Chen, Xiaohu Wang, Yipin Zhao, Chong Chen, Yuhao Liu","doi":"10.3389/fcvm.2025.1526798","DOIUrl":"10.3389/fcvm.2025.1526798","url":null,"abstract":"<p><p>Two years ago, the patient suffered from type A aortic dissection. As a result, partial aortic dissection artificial vascular replacement and partial aortic arch artificial vascular replacement were performed. Six months after the operation, an anastomotic fistula in the ascending aorta was detected, which subsequently progressed to chronic heart failure of New York Heart Association (NYHA grade) class III. After eliminating the operation - related contraindications, the patient successfully had the fistula occluded through transcatheter ascending aorta - right atrial fistula in our hospital. After the operation, no abnormal shunt was found, and the short - term treatment effect was satisfactory.</p>","PeriodicalId":12414,"journal":{"name":"Frontiers in Cardiovascular Medicine","volume":"12 ","pages":"1526798"},"PeriodicalIF":2.8,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11896982/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Burden, risk factors, and projections of ischemic heart disease in China (1990-2021): findings from the 2021 GBD study.","authors":"Sikai Xu, Zhiyang Liu, Mu Tang, Chunli Xu","doi":"10.3389/fcvm.2025.1549147","DOIUrl":"10.3389/fcvm.2025.1549147","url":null,"abstract":"<p><strong>Background: </strong>Ischemic heart disease (IHD) remains a major public health challenge in China. This study aimed to comprehensively analyze the burden of IHD, its risk factors, and future trends from 1990 to 2021 using the Global Burden of Disease database.</p><p><strong>Methods: </strong>We assessed IHD trends in incidence, prevalence, mortality, and disability-adjusted life years (DALYs) stratified by age (greater than 15 years) and gender. Age-standardized rates, average annual percentage changes, and joinpoint regression analyses were used to evaluate temporal trends. Decomposition and frontier analyses were conducted to identify key contributors to the IHD burden, while future projections were generated for the next 15 years.</p><p><strong>Results: </strong>In 2021, the number of IHD incident cases, prevalent cases, deaths, and DALYs in China were 3.17, 3.25, 3.57, and 2.62 times higher than those in 1990, respectively. Age-standardized mortality rates and age-standardized DALYs rates demonstrated an initial increase, followed by a gradual decline. Males showed higher IHD burden during middle age, while elderly females surpassed males in the later years. Aging, high systolic blood pressure, ambient particulate matter pollution, elevated low-density lipoprotein cholesterol, and smoking were the primary drivers of IHD burden. Future projections suggest a declining incidence and prevalence among males but increasing trends in females, with DALYs expected to rise significantly in the female population.</p><p><strong>Conclusions: </strong>The burden of IHD in China has evolved significantly over the past three decades, driven by demographic and environmental factors. While prevalence and incidence have risen, mortality and DALYs have shown a recent decline, reflecting shifts in disease patterns. Age and gender disparities are evident, with middle-aged males and elderly females disproportionately affected. Key contributors, such as high blood pressure and pollution, highlight the need for targeted interventions. Gender-specific public health strategies, alongside improved environmental and health policies, are essential to mitigating the future burden of IHD in China.</p>","PeriodicalId":12414,"journal":{"name":"Frontiers in Cardiovascular Medicine","volume":"12 ","pages":"1549147"},"PeriodicalIF":2.8,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897495/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioinformatics analysis of the expression of potential common genes and immune-related genes between atrial fibrillation and chronic kidney disease.","authors":"Jieying Teng, Guoxiong Deng","doi":"10.3389/fcvm.2025.1521722","DOIUrl":"10.3389/fcvm.2025.1521722","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Research objective: &lt;/strong&gt;This study is based on bioinformatics analysis to explore the co-expressed differentially expressed genes (DEGs) between atrial fibrillation (AF) and chronic kidney disease (CKD), identify the biomarkers for the occurrence and development of the two diseases, investigate the potential connections between AF and CKD, and explore the associations with immune cells.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We downloaded Two AF gene chip datasets (GSE79768, GSE14975) and two CKD gene chip datasets (GSE37171, GSE120683) from the GEO database. After pre-processing and standardizing the datasets, two DEGs datasets were obtained. The DEGs were screened using R language, and the intersection was taken through Venn diagrams to obtain the co-expressed DEGs of AF and CKD. To obtain the signal pathways where the co-expressed DEGs were significantly enriched, GO/KEGG enrichment analyses were used to analysis the co-expressed DEGs. The Cytoscape software was used to further construct a PPI network and screen key characteristic genes, and the top 15 co-expressed DEGs were screened through the topological algorithm MCC. To further screen key characteristic genes, two machine-learning algorithms, LASSO regression and RF algorithm, were performed to screen key characteristic genes for the two disease datasets respectively to determine the diagnostic values of the characteristic genes in the two diseases. The GeneMANIA online database and Networkanalyst platform were used to construct gene-gene and TFs-gene interaction network diagrams respectively to predict gene functions and find key transcription factors. Finally, the correlation between key genes and immune cell subtypes was performed by Spearman analysis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Research results: &lt;/strong&gt;A total of 425 DEGs were screened out from the AF dataset, and 4,128 DEGs were screened out from the CKD dataset. After taking the intersection of the two, 82 co-expressed DEGs were obtained. The results of GO enrichment analysis of DEGs showed that the genes were mainly enriched in biological processes such as secretory granule lumen, blood microparticles, complement binding, and antigen binding. KEGG functional enrichment analysis indicated that the genes were mainly enriched in pathways such as the complement coagulation cascade, systemic lupus erythematosus, and Staphylococcus aureus infection. The top 15 DEGs were obtained through the MCC topological algorithm of Cytoscape software. Subsequently, based on LASSO regression and RF algorithm, the key characteristic genes of the 15 co-expressed DEGs of AF and CKD were further screened, and by taking the intersection through Venn diagrams, five key characteristic genes were finally obtained: PPBP, CXCL1, LRRK2, RGS18, RSAD2. ROC curves were constructed to calculate the area under the curve to verify the diagnostic efficacy of the key characteristic genes for diseases. The results showed that RSAD2 had the highest diagnostic value for AF, ","PeriodicalId":12414,"journal":{"name":"Frontiers in Cardiovascular Medicine","volume":"12 ","pages":"1521722"},"PeriodicalIF":2.8,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"cMyBP-C in hypertrophic cardiomyopathy: gene therapy and small-molecule innovations.","authors":"Patrick T Wood, Morgan M Seffrood, Brett A Colson, Julian E Stelzer","doi":"10.3389/fcvm.2025.1550649","DOIUrl":"10.3389/fcvm.2025.1550649","url":null,"abstract":"<p><p>Hypertrophic cardiomyopathy (HCM) is a genetic disorder in the heart caused by variants in sarcomeric proteins that disrupt myocardial function, leading to hypercontractility, hypertrophy, and fibrosis. Optimal cardiac function relies on the precise coordination of thin and thick filament proteins that control the timing, magnitude of cellular force generation and relaxation, and <i>in vivo</i> systolic and diastolic function. Sarcomeric proteins, such as cardiac myosin binding protein C (cMyBP-C) play a crucial role in myocardial contractile function by modulating actomyosin interactions. Genetic variants in cMyBP-C are a frequent cause of HCM, highlighting its importance in cardiac health. This review explores the molecular mechanisms underpinning HCM and the rapidly advancing field of HCM translational research, including gene therapy and small-molecule interventions targeting sarcomere function. We will highlight novel approaches, including gene therapy using recombinant AAV vectors and small-molecule drugs targeting sarcomere function.</p>","PeriodicalId":12414,"journal":{"name":"Frontiers in Cardiovascular Medicine","volume":"12 ","pages":"1550649"},"PeriodicalIF":2.8,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11935118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A giant and rapid myocardial remodeling due to fatal giant cell myocarditis: a case report.","authors":"Wei Zhang, Tao Guo","doi":"10.3389/fcvm.2025.1488503","DOIUrl":"10.3389/fcvm.2025.1488503","url":null,"abstract":"<p><p>Giant cell myocarditis is a rare and rapidly progressive disease with a high mortality rate. We present the case of a 21-year-old male without a medical history who presented with a giant left ventricle (9.9 cm, EF:10%) and in a severe clinical state. Cardiac MRI and virology raised the suspicion of giant cell myocarditis. Concerned about the hemodynamic and respiratory deterioration, we initiated cardiac transplant therapy. A fatal ventricular fibrillation occurs while waiting for the heart transplant. Sudden death could represent the \"first symptom\" of pathological findings. It is important to recognize that while sudden death due to giant cell myocarditis may be rare, it is still a potentially serious complication of giant cell infection and should be considered in cases of unexplained sudden death. In addition, this case highlights the challenges in the diagnosis and management of giant cell myocarditis and the need for early recognition and aggressive treatment.</p>","PeriodicalId":12414,"journal":{"name":"Frontiers in Cardiovascular Medicine","volume":"12 ","pages":"1488503"},"PeriodicalIF":2.8,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of HDAC2 inhibition in cardioprotection against doxorubicin-induced myocardial injury.","authors":"Jinsha Liu, Wenwen Fu, Xue Wang, Zuowen Liang, Fanbo Meng","doi":"10.3389/fcvm.2025.1557119","DOIUrl":"10.3389/fcvm.2025.1557119","url":null,"abstract":"<p><strong>Introduction: </strong>The molecular mechanisms underlying cardioprotection against doxorubicin (DOX)-induced myocardial injury are poorly understood. Histone deacetylase 2 (HDAC2) plays a significant role in oxidative stress, apoptosis, and mitochondrial dysfunction and is implicated in many human diseases, This study investigated the relationship between HDAC2 expression and DOX-induced myocardial injury using the <i>in vivo</i> rat model of DOX-induced cardiotoxicity and <i>in vitro</i> experiments with the H9c2 cardiomyocytes.</p><p><strong>Methods: </strong>The rat model of DOX-induced myocardial injury was established by administering DOX via intraperitoneal injections. HDAC2 expression was suppressed by administering rats with sodium butyrate (SB) via intraperitoneal injections. Echocardiography measurements were performed at baseline and on day 15 post-treatment. The rats were euthanized on day 15 and cardiac tissues were harvested. The cardiac tissue samples were analyzed by hematoxylin and eosin H&E staining, immunohistochemistry, Masson staining, Sirius Red staining, TUNEL staining, and western blotting to determine the status of HDAC2 expression and myocardial apoptosis. In the vitro experiments, H9c2 cells were treated with DOX. HDAC2 expression was suppressed using sodium butyrate or transfected cells with the shRNA knockdown HDAC2 (shHDAC2). The H9c2 cells from different groups were analyzed by Rt-qPCR, CCK-8 cell viability assay, and western blotting to determine the status of HDAC2 expression and cardiomyocyte apoptosis.</p><p><strong>Results: </strong>DOX treatment induced cardiac dysfunction in rats. The cardiac tissues of the DOX-treated rats and H9c2 cells showed significantly higher levels of HDAC2 compared to the corresponding controls. However, inhibition of HDAC2 significantly mitigated DOX-induced myocardial injury in rats. This suggested a strong association between HDAC2 expression and DOX-induced myocardial injury. In the H9c2 cells, HDAC2 knockdown by shHDAC2 alleviated DOX-induced apoptosis by enhacing AKT phosphorylation. These findings demonstrated that HDAC2 silencing protected against DOX-induced cardiomyocyte apoptosis by activating the PI3K/AKT signaling pathway.</p><p><strong>Conclusion: </strong>Suppressing HDAC2 protected against DOX-induced cardiomyocyte apoptosis by activating the PI3K/AKT signaling pathway. Therefore, HDAC2 is a promising therapeutic target for mitigating DOX-induced myocardial injury.</p>","PeriodicalId":12414,"journal":{"name":"Frontiers in Cardiovascular Medicine","volume":"12 ","pages":"1557119"},"PeriodicalIF":2.8,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aortic endograft infection after thoracic endovascular aortic repair: two case reports and literature review.","authors":"Danping Peng, Guang Xu, Bin Wang, Xin Li, Yang Wang","doi":"10.3389/fcvm.2025.1549613","DOIUrl":"10.3389/fcvm.2025.1549613","url":null,"abstract":"<p><p>With the maturity of thoracic endovascular aortic repair (TEVAR) technology and its increasing application in clinical practice, complications and long-term management after TEVAR have become issues of concern. Here, we report two cases of TEVAR for thoracic aortic dissection. One patient developed recurrent fever 6 years after TEVAR and underwent multiple courses of antibiotic therapy with a poor response. He came to our hospital 6 months later and presented with gastrointestinal bleeding. Imaging revealed the presence of an aortic abscess around the stent graft involving the esophagus and mediastinum. The patient's condition deteriorated rapidly after admission, and he ultimately succumbed to hemorrhagic shock. Another patient developed recurrent fever 1 year after surgery. Imaging studies suggested an aortic abscess with involvement of the esophagus, and the patient chose conservative treatment. After long-term anti-infective treatment, the infected lesions remained but had decreased in size. Aortic endograft infection complicated by multiple organ involvement is a rare complication of TEVAR and has a high mortality rate. After an extended postsurgical period, patients who have undergone TEVAR often lack regular follow-up and are easily overlooked. Our cases highlight the importance of early prevention, early diagnosis, and appropriate management of late complications following TEVAR.</p>","PeriodicalId":12414,"journal":{"name":"Frontiers in Cardiovascular Medicine","volume":"12 ","pages":"1549613"},"PeriodicalIF":2.8,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893612/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}